Valvular Heart Disease

Abstract

VHD (stenosis, insufficiency, or combined lesions) is a major class of heart disease; if severe and left untreated, it may lead to irreversible myocardial damage and death. VHD may exert its deleterious effect both by a direct decrease of stroke volume (e.g., with critical AS or acute severe MR) and by the ultimately deleterious adaptive cardiac changes it produces (ventricular hypertrophy and dilatation, atrial dilatation, and functional or organic PAH). While preventing symptoms despite severe valvular dysfunction, these changes may lead to irreversible myocardial damage. The different types of VHD may cause systolic and diastolic LV dysfunction and failure; infective endocarditis (IE); PAH; AF or flutter and thromboembolic complications; absolute and relative myocardial ischemia and a tendency to develop larger MI; and the iatrogenic complications related to mechanical valvular prostheses. Most cases of chronic VHD have an insidious evolution, occasionally leading to late diagnosis and increased morbidity and mortality; therefore, careful routine physical examination remains the main screening modality for VHD. The typical clinical sign of VHD is a systolic or diastolic heart murmur. Systolic murmurs reflect increased flow velocity through a normal or pathologic connection (cardiac valve, fistula, VSD, etc.) between chambers under different pressures. Thus, high blood flow velocity due to either normal (exercise, pregnancy, etc.) or pathologic states (valve stenosis) may cause a systolic murmur. Most systolic murmurs associate a low probability of underlying disease (“innocent” murmurs, transmitted through the thin chest wall of younger patients); systolic murmurs only require work-up if they have characteristics suggesting increased severity (long, loud murmurs, murmurs associating a thrill, etc.). Conversely, diastolic murmurs are most often pathologic and do require work-up. Continuous murmurs may be innocent (venous hums, mammary souffles) or pathologic (e.g., coronary fistula). The auscultatory characteristics of murmurs include timing in the cardiac cycle, intensity, location, radiation, and quality. Finer characterization distinguishes different murmur configurations (crescendo, decrescendo, crescendo–decrescendo, or plateau). The timing of a systolic murmur is important, most innocent murmurs being midsystolic; holo or late-systolic murmurs are often pathologic. Of note, the length of the murmur per se may be related to the severity of the underlying condition (e.g., longer murmur in severe AS) or not connected to it (early systolic murmur in acute MR; early- and midsystolic murmur only, rather than holosystolic murmur, in large VSD). Likewise, the intensity of the murmur may be directly related to the severity (i.e., loud systolic murmur in severe chronic MR), unrelated to it (loud systolic murmur in hemodynamically insignificant aortic sclerosis, which may be mistaken for AS), or inversely related (loud systolic murmur in small, i.e., nonsevere VSD) to the severity of the underlying heart disease. Usually, the intensity is graded between grades I and VI (grade I = barely audible; grade ≥ IV = associates a palpatory thrill; grade VI = heard even with the stethoscope not immediately touching the skin). The radiation of a mitral systolic murmur is to the left axilla; of an AS murmur, to the left carotid artery; and of a small VSD, to the entire precordium. In contrast, diastolic murmurs tend not to radiate. The quality is described as musical (MR murmur due to papillary muscle dysfunction); blowing (other chronic MR); high-pitched and faint (AI); harsh/rasping (AS); rumbling (low-pitch murmur of MS); or machine-like (“to-and-fro murmur,” e.g., with PDA). Occasionally, different interventions are used to alter the intensity of cardiac murmurs, as reviewed in Table 5.1. Additional diagnostic findings in VHD pertain to the heart sounds, as reviewed in Table 5.2.